增强微管活性改善轴突再生抑制驱动蛋白-5的作用.docVIP

增强微管活性改善轴突再生：抑制驱动蛋白-5的作用 受损的成年轴突可以再生，但它们的再生能力是相当有限的，尤其是在中枢神经系统内。成人中枢神经系统中的受损轴突会趋于回缩或者变性，而不是再生。这是因为受损轴突遇到的物理和化学障碍，如瘢痕组织和损伤相关抑制分子，因为成人中枢神经系统环境通常富含的因子如髓鞘是不利于再生的，并且成人轴突固有的生长潜力与幼年轴突并不匹配。 来自美国德雷克塞尔大学医学院Peter W. Baas教授表示，在最近几年，出现了专注于研究微管用于增强损伤成年轴突再生能力的最有希望的目标。微管、微管蛋白亚单位的中空聚合物长丝，为轴突提供结构支撑，并作为许多分子运动蛋白的基板，负责细胞内运输。微管在本质上是极性结构，每一个正端均与负端相配。分子运动蛋白表达的运载物，如沿微管的晶格膜细胞器，特别是朝向其正负端取决于特定的运动蛋白。相关内容发表在2015年6月第6期《中国神经再生研究（英文版）》杂志上。 Article: Inhibition of kinesin-5 improves regeneration of injured axons by a novel microtubule-based mechanism by Peter W. Baas, Andrew J. Matamoros (Department of Neurobiology and Anatomy, Drexel University College of Medicine, 2900 Queen Lane, Philadelphia, PA, USA) Baas PW, Matamoros AJ (2015) Inhibition of kinesin-5 improves regeneration of injured axons by a novel microtubule-based mechanism. Neural Regen Res 10(6):845-849. 欲获更多资讯：/ Inhibition of kinesin-5 improves regeneration of injured axons by a novel microtubule-based mechanism Microtubules have been identified as a powerful target for augmenting regeneration of injured adult axons in the central nervous system. Drugs that stabilize microtubules have shown some promise, but there are concerns that abnormally stabilizing microtubules may have only limited benefits for regeneration, while at the same time may be detrimental to the normal work that microtubules perform for the axon. Prof. Peter W. Baas focused on Kinesin-5 (also called kif11 or Eg5), a molecular motor protein best known for its crucial role in mitosis, acts as a brake on microtubule movements by other motor proteins in the axon. Drugs that inhibit kinesin-5, originally developed to treat cancer, result in greater mobility of microtubules in the axon and an overall shift in the forces on the microtubule array. As a result, the axon grows faster, retracts less, and more readily enters environments that are inhibitory to axonal regeneration. Thus, drugs that inhibit kinesin-5 offer a novel microtubule-based means to boost axonal regeneratio